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Friday, March 13, 2015 9:28 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Wish to understand MS?...Truly? - which one?, by Dr. Franz Schelling

Faceless MS?

Clinically defined CDMS?

Nerve dysfunctions, deemed diagnostic, provided they
• have no known cause,
• persist, in between pause, for set periods of time.

Devoid of substance, form, any physical or organic property, this multiple sclerosis has but its red flags of what it must not be mistaken for. It decently hides the nature of the changes it represents.

Inflammatory demyelinating or 'ADEM-EAE' MS?

Natural acute disseminated encephalomyelitis(ADEM) and its experimental allergic counterpart EAE is millet to pea-sized longish foci or rather sleeves formed round blood vessels in the course of inflammatory reactions.
They mark some circulated agent's/s' spread.

A Rindfleisch case report of 1863 led to no little confusion in relating this pathology to (uncited) Rokitansky accounts on a certain actively injurious sclerosing process of spinal cord and brain.

But no MS-specific inflammatory demyelination, no MS set apart by some feature(s) of ADEM of EAE has ever been identified.
No circulated agent can be imagined to invade spinal cord and brain in the ways MS lesions spread (Steiner 1931).

From a pragmatist standpoint, CDMS associated 'ADEM-EAE' [MS] may still be viewed a clinically convenient explanatory construct.

Is this clinically defined inflammatory demyelinating MS worth research efforts and time?

For heaven's sake, NO!

Two-natured MS?

From Carswell(1831) to Oppenheim(1978) autopsies detected ever new findings peculiar to spinal MS.
In the brain radically different yet equally distinctive changes came to be pictured since the days of Charcot(1866) at post mortem, then routinely, even serially, in vivo on MRIs, in the wake of Young ea's observations of 1981.

The findings, puzzling in themselves, resist being fitted together into a coherent whole unless one and the other are understood separately.

A distinct picture emerges of how cerebral and spinal MS evolve, but understanding the two natures of MS requires

• Acquaintance with some clearly shown and yet widely missed facts

https://medium.com/@franzschelling/open-letter-to-cedric-s-raine-bc1df79b106d,

• Riddance of misleading doctrines

https://medium.com/@franzschelling

• Facing up to the apparently paradoxical ways in which brain and cord lesions advance

www.ms-info.net

Ridiculous?

But how else appreciate that:

(A) Venous wetterwinkel/corpus callosum MS lesions mirror those of traumatic brain injury (TBI)
https://dl.dropboxusercontent.com/u/66292082/MS%20WETTERWINKEL%20LESIONS%20PARALLEL%20TRAUMATIC%20BRAIN%20INJURY.pdf

(B) Mooring lesions of traumatic spinal cord injury (TSCI) so closely mimic spinal MS?

(C) MS reflects a concussive injuring of brain and/or spinal core by sporadic intolerable expansions of veins in the brain respectively spinal canal?

With MRI time-lapse series of MS patients that show
• A 'cockscomb'(Heckl 1994) lesion growth along and off the outer angle of a lateral ventricle, or plaques(Steiner 1931), hemorrhages spread in the same way,attended by
• Engorgements, then shrinking of local veins .....
• A sclerosing process invading the spinal cord from insertion zones of mainly the denticulate ligament .....
The attribution of multiple sclerosis to a fusion of perivenular lesion sleeves is patently absurd .....may be except to those who feel obliged to keep up a fatal status quo.

Dr. Franz Schelling